FIGURE 19.1

Human immunodeficiency virus (HIV) infection. HIV enters the Langerhans dendritic cell, via gp120 binding to the receptors CD4 and CCR5; HIV then spreads to the T cells via the same receptors, and throughout the lymphoid system. Over time, the virus mutates and enters T cells via CD4 and CXCR4 receptors.

FIGURE 19.2

Typical time course of HIV/AIDS, without antiretroviral therapy.

FIGURE 19.3

Overview of HIV infection and clinical outcome.

FIGURE 19.4

The progression of HIV disease. As the immune system is destroyed, the more virulent opportunist infections (e.g. tuberculosis) develop earlier, and the less virulent (e.g. M. avium-intracellulare) later.

FIGURE 19.5

Cytomegalovirus (CMV) pneumonitis: large intranuclear viral inclusions in alveolar epithelial cells.

FIGURE 19.6

Herpes simplex virus (HSV) of the penis: eroded squamous mucosa with multinucleated cells, the nuclei containing blocks of HSV virions.

FIGURE 19.7

Pneumocystis jirovecii pneumonia: complete consolidation of the lung.

FIGURE 19.8

Pneumocystis jirovecii pneumonia: the alveoli are filled with numerous tiny cysts with nuclear dots. Interstitial inflammation is present.

FIGURE 19.9

Cryptococcal CNS disease: within the white and grey matter are ‘holes’ – these are large accumulations of Cryptococcus neoformans.

FIGURE 19.10

Kaposi’s sarcoma: widespread nodular lesions around the pelvis, with leg oedema, in an HIV-infected young man.

FIGURE 19.11

HIV encephalitis: microglia and giant cells in the cerebral white matter.

FIGURE 19.12

Cryptosporidiosis. Right: oocysts of Cryptosporidium in the faeces (Ziehl–Neelsen staining). Left: rectal crypt lined by numerous parasites.

FIGURE 19.13

Cerebral toxoplasmosis: haemorrhagic necrotic lesion compressing the brain.

FIGURE 19.14

The typical development of tuberculosis (TB); primary complex, miliary TB and subsequent post-primary pulmonary TB. The immunopathological inputs are indicated: CMI (cell-mediated immunity) and DTH (delayed-type hypersensitivity). AFB = acid-fast bacilli.

FIGURE 19.15

Primary tuberculosis in a child: the small lung lesion near the left apex, and the large hilar node caseating masses are seen.

FIGURE 19.16

Schematic outline of cell-mediated immunity. Macrophages present antigens to a CD4 + T cell via MHC class II molecules, while cytokines activate macrophages to epithelioid cells. The alternative activation route via NK cells is indicated. IFN = interferon; IL = interleukin; TNF = tumor necrosis factor.

FIGURE 19.17

Caseation of a lymph node in primary tuberculosis, with surrounding giant cell granulomas.

FIGURE 19.18

Post-primary pulmonary tuberculosis: cavitating lesions at the apex and elsewhere.

FIGURE 19.19

Miliary tuberculosis in the lung: numerous small white necrotic lesions in parenchyma and the hilar node.

FIGURE 19.20

Pulmonary lesions: necrotic macrophages, and no granulomas.

FIGURE 19.21

Acid-fast staining to show vast numbers of tubercle bacilli. (Ziehl–Neelsen.)

FIGURE 19.22

MAI infection. Left: duodenal biopsy with macrophages filling the lamina propria. (Haematoxylin and eosin staining.) Right: the cells contain many acid-fast bacilli (AFB). (Ziehl–Neelsen.)

FIGURE 19.23

Leprosy: outcome of infection and the basic immunopathology.

FIGURE 19.24

Clinical leprosy. (A) Lepromatous widespread nodular lesions. (B) Tuberculoid leprosy with few, hypopigmented flat lesions.

FIGURE 19.25

Lepromatous leprosy of the skin: packed macrophages under the epidermis.

FIGURE 19.26

Lepromatous leprosy: macrophages contain many acid-fast leprosy bacilli. (Wade–Fite.)

FIGURE 19.27

Tuberculoid leprosy: skin biopsy showing a deep nerve disrupted by a giant cell granulomatous infiltrate.

FIGURE 19.28

Spirochaetes of Treponema pallidum in congenital syphilis. (Warthin–Starry.)

FIGURE 19.29

Sequelae of events in untreated syphilis, with time scales and approximate proportions. GPI = general paralysis of the insane.

FIGURE 19.30

Oesophageal candidiasis: note the thick coat of fungus on the mucosa.

FIGURE 19.31

Oesophageal candidiasis: fungal hyphae invading the mucosa. (Grocott silver.)

FIGURE 19.32

Invasive aspergillosis: fungal hyphae infiltrating the bronchial
wall.

FIGURE 19.33

Mycetoma of the foot: swelling and discharging sinuses.

FIGURE 19.34

Sequelae of infection with Plasmodium falciparum causing malaria. TNF = tumour necrosis factor.

FIGURE 19.35

Malarial liver: note the extensive brown haemozoin pigment in Kupffer cells and portal macrophages.

FIGURE 19.36

Cerebral malaria in a child: mild swelling, grey cortex (from the haemozoin pigment) and petechial haemorrhages in the white matter.

FIGURE 19.37

Pathogenesis of sequestration in falciparum malaria. ICAM = intercellular cell adhesion molecule; RBC = red blood cell; TNF = tumour necrosis factor.

FIGURE 19.38

Red cell with falciparum malaria: this scanning electron micrograph shows the tiny knobs on the red cell surface.

FIGURE 19.39

Plasmodium falciparum infection of red cells: the blood smear shows many ring forms in red cells. (Giemsa.)

FIGURE 19.40

Cerebral malaria: capillaries with sequestration of parasitized red cells.

FIGURE 19.41

Visceral leishmaniasis: bone marrow biopsy with many parasites in the macrophages.

FIGURE 19.42

Giardiasis: six pear-shaped parasites near the enterocyte surface.

FIGURE 19.43

Sequelae of infection with Entamoeba histolytica.

FIGURE 19.44

Amoebiasis: caecum with many ulcers.

FIGURE 19.45

Amoebiasis: trophozoites (many with phagocytosed red cells) invading under the colon mucosa.

FIGURE 19.46

Amoebiasis: four liver abscesses are indicated.

FIGURE 19.47

The pathogenesis of intestinal amoebiasis: the parasites secrete a potent ionophore (‘amebapore’) which results in lysis of the cell.

FIGURE 19.48

Sequelae of infection with Toxoplasma gondii.

FIGURE 19.49

Cerebral toxoplasmosis: a cyst breaking up (left), with many tiny parasites, spreading through the brain.

FIGURE 19.50

Sequence of clinicopathological events in schistosomiasis.

FIGURE 19.51

Schistosoma haematobium: live eggs in a mucosa.

FIGURE 19.52

Schistosoma mansoni: chronic liver infection has caused marked fibrosis around the main portal tracts.

FIGURE 19.53

Schistosoma mansoni: chronic liver infection with two granulomas surrounded by concentric fibrous rings, and increased portal fibrosis tissue linking them. (van Gieson.)

FIGURE 19.54

Hydatid cysts in the mesentery, causing intestinal obstruction.

FIGURE 19.55

Hydatid cyst: the pale-staining laminated membrane (bottom), germinal membrane (red line) and numerous scolices within the cyst.

FIGURE 19.56

Sequelae of infection with Strongyloides stercoralis.

FIGURE 19.57

Strongyloides hyperinfection: small bowel with heavy infection of adult and larval worms in the mucosa.

FIGURE 19.58

Septic shock: the sequelae of events. DIC = disseminated intravascular coagulation; IL = interleukin; LPS = lipopolysaccharide; NO = nitric oxide; TNF  =tumour necrosis factor.

FIGURE 19.59

Lung: the pulmonary arteriole (lower half) is thickened from infiltrating Pseudomonas bacilli, and thrombosed; the surrounding lung is infarcted.

FIGURE 19.60

Kidney: thrombi in the glomerular capillaries, indicating disseminated intravascular coagulation.